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Respiratory Physiology Flashcards

1
Q

What cranial nerve innervates the superior and inferior surfaces of the hard and soft palate?

A

palatine nerves (sensory fibers from the trigeminal (V) nerve)

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2
Q

What cranial nerve innervates the anterior two-thirds of the tongue?

A

lingual nerve, a branch of the mandibular division (V3) of the trigeminal nerve

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3
Q

What cranial nerve innervates the posterior one-third of the tongue?

A

glossopharyngeal (IX) nerve

Also innervates the roof of the pharynx, the tonsils, and the undersurface of the soft palate.

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4
Q

What nerve provides taste to the tongue?

A

facial (VII) nerve (chord tympani) anteriorly

glossopharyngeal (IX) nerve posteriorly

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5
Q

What does the external branch of the superior laryngeal nerve (vagus) supply?

A

Motor to cricothyroid

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6
Q

What does the internal branch of the superior laryngeal nerve (vagus) supply?

A

SENSORY to the larynx b/w the epiglottis and the vocal cords and to the HYPOPHARYNX posterior to those structures

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7
Q

What does the recurrent laryngeal branch of the vagus nerve supply?

A

SENSORY to the larynx below the vocal cords and the trachea

Motor to all of the laryngeal muscles EXCEPT the cricothyroid muscle (external branch of superior laryngeal n.)

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8
Q

Where does the larynx start and end?

A

epiglottis –> cricoid cartilages

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9
Q

How many laryngeal cartilages are there and what are their names?

A

9 cartilages:

3 single cartilages (thyroid, cricoid, epiglottic)

3 paired cartilages (arytenoid, corniculate, and cuneiform)

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10
Q

What cartilages forms the only complete ring in the upper airway?

A

cricoid

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11
Q

The position of which artery needs to be considered when planning a cricothyrotomy?

A

Superior cricothyroid arteries in upper 1/3 of cricothyroid membrane crossing horizontally

Carotid –> superior and inferior thyroid arteries –> laryngeal branches

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12
Q

Which is the only abductor muscle of the vocal cords?

A

posterior arytenoid muscles (lateral = adductors)

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13
Q

List the 6 major anatomic differences between the infant and adult airway.

A
  1. infant’s tongue is relatively large in proportion to the rest of the oral cavity –> more frequent airway obstruction
  2. infant’s occiput is relatively large compared to the rest of the body –> anterior flexion of the head when supine (small shoulder roll can improve the alignment of the head)
  3. infant’s larynx is more cephalad - level of C3-4, vs. level of C4-5 in an adult –> more acute angle from the oral axis to the tracheal axis and may result in more difficulty visualizing the larynx during laryngoscopy
  4. adult’s epiglottis is flat and broad vs. infant’s epiglottis is narrower, omega shaped, and more floppy –> more difficult to lift the infant’s epiglottis with the tip of the laryngoscope blade
  5. infant’s vocal cords more caudad attachment anteriorly than posteriorly (adult, the vocal cord axis is perpendicular to the trachea) –> during intubation of an infant, ETT may get caught at junction of the anterior commissure and epiglottis and not pass into the trachea.
  6. narrowest part of an infant’s larynx = cricoid cartilage (equal in an adult). Must ensure the ETT chosen is the right size and that there IS a leak around the ETT. The differences between the pediatric airway and adult airway persist until approximately 8 years of age.
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14
Q

What cervical and thoracic vertebral landmarks mark the course of the trachea?

A

C6 –> Sternal angle/T5

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15
Q

During respiration, when are the external intercostal muscles most active?

A

Inhalation - responsible for 25% of Tv during quiet breathing (diaphragm 70%) - run forward and downward

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16
Q

What structures pass through the diaphragm at T8, T10, T12?

A

T8 = IVC

T10 = Esophagus

T12 = Aorta, thoracic duct, azygous vein

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17
Q

What is the difference between dynamic and static compliance?

A

Static compliance = change in volume for a given pressure when there is no air flow.

  • measured at end inspiration when flow stops = plateau pressure used to calculate compliance

Dynamic compliance = compliance during a period of air flow - always

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18
Q

What are the two primary factors that affect static lung compliance

A
  1. tissue elasticity - dec in fibrosis, and excess internal or external thoracic pressures (pneumothorax, hydrothorax, abdominal insufflation, obesity, etc.)
  2. surface tension
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19
Q

How does dynamic lung compliance change with lung volume?

A
  • best when lung volumes are moderate
  • worsens dramatically at extremes of low or high lung volumes - low lung volumes = alveoli are collapsed
  • high lung volumes = alveoli are stretched
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20
Q

What is the function of surfactant?

A

it lessens the surface tension, making it less likely that the alveolus will collapse

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21
Q

What size alveolus does surfactant benefit the most and why?

A

Small alveolus Smaller = greater inward pressure pressure (Law of Laplace)

Surfactant reduces the surface tension on every alveolus, but its effect is greater on small alveoli than on large alveoli.

Thus, surfactant compensates for the size differences between alveoli, and ensures that the smaller alveoli do not readily collapse.

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22
Q

What is the Law of Laplace?

A

trans-alveolar pressure gradient = inversely proportional to the alveolar radius, and directly proportional to surface tension.

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23
Q

What is the pleural pressure gradient?

A

difference b/w alveolar pressure and intrapleural pressure of the lungs.

During ventilation, air flows because of this pressure gradient.

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24
Q

For a given pressure, is lung volume greater during inspiration or expiration? (Hysteresis)

A

Expiration

The difference in compliance is due to the additional energy required during inspiration to recruit and inflate additional alveoli.

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25
Q

What factor contributes most to respiratory flow resistance?

A

The flow resistance of the major conducting airways and is dependent upon their radius.

Others: smooth muscle tone (bronchospasm/inflammation) foreign bodies compression of airways turbulent gas flow airway equipment such as endotracheal tubes and connectors.

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26
Q

What is a common cause of increased peak pressures but with normal plateau pressure?

A

Bronchospasm

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27
Q

What factors affect diffusion of gases across the alveolar membrane?

A

hemoglobin concentration alveolar partial pressures of gases body position pulmonary capillary red blood cell volume

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28
Q

What factors influence the diffusing capacity of gases between the blood and the lungs?

A

alveolar membrane thickness

surface area

permeability

interstitial space between the alveolus and capillary

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29
Q

What preoperative predicted DLCO is associated with poor postoperative outcomes?

A

DLCO of <40%

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30
Q

What is the primary stimulus for ventilation at the: 1. central medullary chemoreceptors? 2. peripheral baroreceptors?

A
  1. changes in pH 2/2 CO2 diffusion across BBB = rise in CO2 –> rise in [H+] (decrease in pH) –> increasing minute ventilation
  2. carotid body and aortic body - changes in O2 tension in the blood –> important role in stimulation of breathing in patients who are chronic CO2 retainers (such as in severe COPD)
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31
Q

How is continuous positive airway pressure (CPAP) able to maintain oxygenation?

A

CPAP maintains an open airway and delivers O2 alveoli remain open + minimal shunting or V/Q mismatch, [O2] in the blood will remain relatively constant

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32
Q

What is the rate of rise in CO2 during the first minute of apnea? And every minute thereafter?

A

6 mmHg CO2 in the first minute

3 mmHg per minute thereafter

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33
Q

Define diffusion hypoxia (“third gas effect” or Fink effect)? How do you prevent this?

A

relatively high solubility of nitrous oxide, as compared to nitrogen (30 times greater) nitrous oxide comes out of blood–> alveoli faster than nitrogen uptake into the alveoli –> dilution of gas in the alveoli as room air (FiO2 21%) enters the system

The resultant lower partial pressure of O2 in the alveolus –> hypoxia.

In healthy patients - very short-lived and of questionable clinical significance, but sicker patients (e.g., advanced COPD) –> more profound and longer-lasting hypoxia

Administration of 100% oxygen for the first several minutes following nitrous oxide discontinuation reliably prevents diffusion hypoxia

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34
Q

What is the Bohr effect?

A

Inc O2 release of Hb in response to higher CO2 tension or lower pH

35
Q

What factors affect diffusion of gases in the lung?

A

[Hb]

Alveolar partial pressure of gases

Body position

Pulmonary capillary bed blood volume (V/Q 1.0)

36
Q

How much oxygen is dissolved in the blood?

A

Dissolved = 3%, rest bound to Hb

carbon monoxide poisoning severe anemia severe shock = the relative contribution of dissolved oxygen to blood oxygen content is higher solubility O2 in plasma is low - proportional to the partial pressure of oxygen in the blood (0.003 * PaO2) –> even large inc in PaO2 have small impact on blood O2 content

37
Q

How is blood oxygen content calculated?

A

CaO2 = Hb x 1.34 x (SaO2/100) + 0.003 x PaO2 1.34 = binding capacity of Hb for O2 or 1.34ml O2 bound /g Hb

38
Q

How is the % saturation of Hb calculated?

A

SaO2 (%) = (oxyHb/totalHb) x 100

39
Q

How do you calculate oxygen consumption?

A

VO2 = CO x (CaO2 - CvO2)

40
Q

What affects CO2 elimination?

A

Alveolar ventilation

Pulmonary blood flow

Diffuses much more readily than O2 and almost totally equilibrates

41
Q

How is CO2 transported in the blood?

A

dissolved CO2 (7%)

bicarbonate ion (70%)

carbaminohemoglobin (23%)

42
Q

What distinguishes the CO2 dissociation curve from the O2 dissociation curve?

A

Blood CO2 = nearly linear, much steeper than O2 dissociation curve = blood carries more CO2 than O2 per unit change in partial pressure

43
Q

How does hypercarbia affect cerebral blood flow?

A

For each 1 mm Hg inc in PaCO2 (from 20 – 80mm Hg):

  1. Cerebral blood flow (CBF) - inc ~1.8 mL / 100 g brain tissue / minute
  2. Cerebral blood volume (CBV) - inc ~0.04 mL / 100 g brain tissue / minute.
44
Q

What effect does hypercarbia have on: 1. pulmonary vascular resistance 2. hypoxic pulmonary vasoconstriction 3. O2-Hb dissociation curve

A
  1. Inc pulm vasc resistance
  2. Inc pulm vasoconstriction
  3. Rightward shift
45
Q

What effect does hypercarbia have on:

  1. cardiovascular sympathetic tone
  2. BP, CO
A
  1. Inc sympathetic tone, inc epi and NE levels
  2. Inc CO and BP until extremes –> dec –> VT/VF
46
Q

What does SaO2 represent?

A

Oxyhemoglobin saturation - % of Hb saturated w/ O2

47
Q

What is the physiologic implication of cooperative oxygen binding by hemoglobin?

A

conformational changes –> affinity of each Hb tetramer for O2 increases as more of the Hb monomers bind to

O2 Gives the O2-Hb dissociation curve its sigmoidal shape –> improves efficiency of O2 delivery

48
Q

Give the corresponding Sa O2 for the following PaO2: 1. 40 2. 50 3. 60

A
  1. PaO2 40 = SaO2 70
  2. PaO2 50 = SaO2 80
  3. PaO2 60 = SaO2 90
49
Q

What things cause a rightward shift of the oxyhemoglobin dissociation curve?

A

dec pH (Bohr effect)

Hypercarbia (Bohr effect)

INC 2,3-DPG

Hyperthermia

Pregnancy HbS - in setting of hypoxia

Thalassemia

Volatile anesthetics

Low Phos

50
Q

Which is a better buffer, oxyhemoglobin or deoxyhemoglobin?

A

deoxyhemoglobin is a better buffer

Carboxyhemoglobin + O2 → oxyhemoglobin + CO2

51
Q

What is the normal P50 and what does a rightward shift of the oxyhemoglobin dissociation curve imply?

A

P50 = 26.8mmHg

Rightward shift = higher P50 = Inc uptake from alveoli + hb unloads O2 to tissues at a higher O2 tension = enhances O2 delivery but DEC O2 RELEASE to tissues

52
Q

What is the importance of the Haldane effect?

A

oxygenation of Hb enhances (doubles) the delivery of CO2 to the alveoli (enhances CO2 elimination)

53
Q

What is functional residual capacity?

A

volume of gas that remains in the lung after the completion of a normal breath.

normally 30–40 mL/kg or approximately 2.5 L

Increase FRC with PEEP

54
Q

What are the dynamic lung volumes and capacities?

A

tidal volume, inspiratory reserve volume, expiratory reserve volume, inspiratory capacity, and vital capacity.

Total lung capacity (TLC) - total volume of gas in the lungs at maximum inspiration

  • normal = 80 mL/kg (6 to 8 L in adults)
  • increased with obstructive lung disease
  • reduced in patients with restrictive lung disease

Tidal volume (TV) - volume of a normal breath.

  • normal = 6 – 8 mL/kg, or approximately 500 mL.
  • increases with activity

Vital capacity (VC) - maximum volume expired after a maximum inspiration.

  • normal = 4 to 6 liters.
  • reduced in both restrictive and obstructive diseases.
55
Q

What are the static lung volumes and capacities?

A

residual volume

total lung capacity

functional residual capacity

can NOT be measured by simple spirometry

must be measured by more complex methods that include inert gas dilution (helium), nitrogen washout, or whole-body plethysmography.

56
Q

What is closing capacity?

A

lung volume below which small airways (beyond the 11th bronchial division with radius from 0.5 to 0.9 mm) start to collapse.

57
Q

What increases the closing capacity?

A

Smoking

obesity

aging

supine position

58
Q

Name some things that decrease a patient’s FRC

A

supine (vs erect) position (by 30-40%)

general anesthesia and surgery (an additional 20-40%)

Upper abdominal surgery = greatest reduction at 40%,

thoracic and lower abdominal = 30% reduction

extremity surgery = 20% reduction

59
Q

An FVC below what is associated with increased post-op complications?

A

<15 ml/kg

60
Q

Describe the FEV1/FVC in obstructive and restrictive lung disease

A
  1. obstructive lung disease = reduced FEV1 (FEV1s / FVC < 75%)
  2. restrictive diseases = normal FEV1 / FVC despite the reduced FEV1
61
Q

A VO2 Max below what is associated with increased post-thoracotomy complications?

A

< 15 mL/kg/min = very high risk of post thoracotomy complications

> 20 mL/kg/min = low chance of post-thoracotomy complications

62
Q

How much pressure needs to be applied during a recruitment maneuver to expand all atelectasis?

A

40cmH2O for 8 seconds

63
Q

Name the two peripheral chemoreceptors and their innervation.

A
  1. Central chemo receptors in Medulla
  2. Peripheral chemoreceptors in carotid body (CN IX), dominant in adults and the aortic body (CN X) - more important in neonates.
64
Q

What are some examples of lung mechanoreceptors and how do they act?

A

vagus nerve

  1. Slowly adapting receptors (SAR)
    1. alter breathing and airway tone
    2. Hering Breuer reflex –> inhibits inspiration and stimulates expiration in response to over inflation of lung.
    3. More important in newborns.
  2. Rapidly adapting receptors (RAR) = mediating cough.
65
Q

At what oxygen tension/partial pressure does the ventilatory response increase?

A

PaO2~100 mmHg - increase in ventilation is minimal (<10% increase) until the PaO2 falls below 70 mmHg

PaO2 of 60 mmHg - minute ventilation ~doubles

Maximal response - PaO2 of approximately 40 mmHg, = minute ventilation has nearly quadrupled

66
Q

Describes the 3 phases of hypoxic ventilatory response

A
  1. Acute hypoxic response (immediate 1- 3 minutes)
    1. carotid bodies and glossopharyngeal nerve
    2. ventilation increases in response to hypoxia
    3. Glutamate mediating this response.
  2. Hypoxic ventilatory decline (3-6 minutes, “roll off”)
    1. higher than normal minute ventilation but lower than the acute response.
    2. GABA mediates the dampening of the acute response.
  3. Acclimatization (slower, prolonged) – excessive erythropoietin.
    1. tremendous stress to maintain ventilatory stimulation to hypoxia for prolonged periods –> kidneys produce erythropoietin –> stimulates RBC production and oxygen carrying capacity.
67
Q

What is the most important chemical stimulant for ventilation?

A

Arterial carbon dioxide partial pressure

68
Q

Where is most of the chemoreceptor drive to increase ventilation mediated?

A

central chemoreceptors = PaCO2

peripheral = PaO2

69
Q

What causes a leftward shift of the CO2 response curve?

A
  1. Arterial hypoxemia.
  2. Metabolic acidemia.
  3. Central nervous system etiologies:
    1. Drugs – aminophylline, doxapram, salicylates, norepinephrine, opioid antagonists (only when given after an opioid!)
    2. Increased ICP
    3. Cirrhosis
    4. Anxiety/fear
  4. Pregnancy.
70
Q

What causes a rightward shift of the CO2 response curve?

A
  1. Metabolic alkalemia
  2. Denervation of peripheral chemoreceptors (e.g. carotid body resection)
  3. Sleep
  4. Drugs – opioid agonists, volatile anesthetics, large doses of barbiturates & benzodiazepines

This means ETCO2 will need to rise to 40 mmHg for him to reach his apneic threshold and start breathing (vs. 32mmHg normally)

71
Q

What is the normal apneic threshold and how is it calculated?

A

~4-5 mmHg below the resting PaCO2

In normal awake adults, the apneic threshold is at a PaCO2 of ~32 mm Hg.

72
Q

Does the dorsal respiratory group of neurons stimulate inspiration or expiration or both?

A

Dorsal = inspiratory only

73
Q

Is the central respiratory pattern rhythm generator located in the medulla or pons?

A

medulla

74
Q

Besides the diaphragm, what is the second most important muscle of inspiration?

A

external intercostal muscles

75
Q

What is bronchoconstriction?

A

smooth muscle contraction –> narrowing of the airways –> to difficulty with expiration.

Clinically - audible expiratory wheezing if some air is moving through the bronchi or severe hypoxemia and respiratory arrest if there is complete obstruction of the airway.

76
Q

What is the mechanism of action of the selective beta 2 receptor agonists?

A

selective beta 2 agonists –> activating adenylate cyclase –> increase the production of cyclic adenine monophosphate (cAMP) from adenine triphosphate (ATP).

cAMP acts to relax the respiratory smooth muscle, resulting in bronchodilation

77
Q

Where do anticholinergics act to cause bronchodilation?

A

Acetylcholine –> muscarinic receptors (specifically M3) in the bronchial smooth muscle–> increase cyclic guanine monophosphate (cGMP) –> smooth muscle to cause bronchoconstriction.

Anticholinergics block acetylcholine, thereby decreasing cGMP, leading to inhibition of reflex bronchoconstriction and overall bronchodilation

78
Q

How do phosphodiesterase inhibitors cause bronchodilation and why are they so difficult to use effectively?

A

block the action of the enzyme phosphodiesterase, thereby preventing cAMP from breaking down –> bronchodilation

very small therapeutic window

Aminophylline - ventricular dysrhythmias from increased release of catecholamines.

Theophylline - nausea/vomiting, arrhythmias, and seizures, interacts with the metabolism of other medications such as antiepileptic medications or antibiotics

79
Q

What is leukotriene?

A

an inflammatory mediator that causes severe bronchoconstriction and promotes airway mucus secretion

80
Q

What is a mast cell stabilizer and is it useful in acute exacerbation of asthma?

A

block the IgE-regulated calcium channel –> preventing intracellular accumulation of calcium –> prevents histamine vesicles –> preventing bronchoconstriction

Not useful for actue asthma treatment, only prevention

81
Q

How do steroids help in the treatment of asthma or COPD?

A

decrease inflammation in the airways that may be causing an acute exacerbation

82
Q

What is the mechanism of action of volatile anesthetics to cause bronchodilation?

A

directly on the smooth muscle of the airways to cause relaxation.

Indirectly - inhibit the vagal nerve reflex that causes bronchoconstriction, thereby causing bronchodilation

83
Q

What spirometric parameter is MOST predictive of pulmonary complications?

A

Ppo FEV1% = preoperative FEV1% x (1 - %functional lung tissue removed/100).

If the Ppo FEV1% > 40%, a patient is at low risk of respiratory complications.

If the ppoFEV1% < 30%, a patient is at high risk of pulmonary complications

84
Q

What second messenger causes bronchodilation? Bronchoconstriction?

A

cAMP = bronchodilation

cGMP = constriction

Anesthesia (25 decks)

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